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    AKI Acute Kidney Injury

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    Via Anggraeni
    This document discusses acute kidney injury (AKI). It provides definitions of AKI, describes the pathogenesis which involves ischemia and inflammation, and lists common signs and symptoms such as azotemia, hypertension, and arrhythmias. It also discusses evaluating for pre-renal, renal, and post-renal causes of AKI. Management principles focus on identifying and correcting underlying factors, optimizing cardiac output, and treating complications. Indications for renal replacement therapy include refractory fluid overload, hyperkalemia, uremia, and metabolic acidosis. Both continuous and intermittent renal replacement therapies are options depending on the clinical situation and resources available.

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    AKI Acute Kidney Injury

    Uploaded by

    Via Anggraeni
    21 views46 pages
    This document discusses acute kidney injury (AKI). It provides definitions of AKI, describes the pathogenesis which involves ischemia and inflammation, and lists common signs and symptoms such as azotemia, hypertension, and arrhythmias. It also discusses evaluating for pre-renal, renal, and post-renal causes of AKI. Management principles focus on identifying and correcting underlying factors, optimizing cardiac output, and treating complications. Indications for renal replacement therapy include refractory fluid overload, hyperkalemia, uremia, and metabolic acidosis. Both continuous and intermittent renal replacement therapies are options depending on the clinical situation and resources available.

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    AKI

    Original Title

    Aki

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    This document discusses acute kidney injury (AKI). It provides definitions of AKI, describes the pathogenesis which involves ischemia and inflammation, and lists common signs and symptoms such as azotemia, hypertension, and arrhythmias. It also discusses evaluating for pre-renal, renal, and post-renal causes of AKI. Management principles focus on identifying and correcting underlying factors, optimizing cardiac output, and treating complications. Indications for renal replacement therapy include refractory fluid overload, hyperkalemia, uremia, and metabolic acidosis. Both continuous and intermittent renal replacement therapies are options depending on the clinical situation and resources available.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    21 views46 pages

    AKI Acute Kidney Injury

    Uploaded by

    Via Anggraeni
    This document discusses acute kidney injury (AKI). It provides definitions of AKI, describes the pathogenesis which involves ischemia and inflammation, and lists common signs and symptoms such as azotemia, hypertension, and arrhythmias. It also discusses evaluating for pre-renal, renal, and post-renal causes of AKI. Management principles focus on identifying and correcting underlying factors, optimizing cardiac output, and treating complications. Indications for renal replacement therapy include refractory fluid overload, hyperkalemia, uremia, and metabolic acidosis. Both continuous and intermittent renal replacement therapies are options depending on the clinical situation and resources available.

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    AKI

    ACUTE KIDNEY INJURY


    AUTOREGULASI

    • Mekanisme miogenik

     Sel otot polos arteriol aferen

     perfusi ginjal meningkat  kontraksi ↑

    • Umpan balik tubuloglomerular


    ACUTE
    KIDNEY INJURY
    BACKGROUND

    • Increasingly common & potentially catastrophic complication in


    hospitalized patients

    • Current prevention strategies are inadequate & current treatment


    options other than RRT nonexistent

    • Diagnostic approach has been stagnant

    • Identification & validation of novel biomarkers for AKI

    •  permit earlier & more accurate diagnosis


    ARFAKI
    • includes the entire spectrum of ARF +

    • minor changes in kidney function (reflected by a change in


    serum creatinine [SCr] of 0.3 mg/dL)

    • the term “failure” renal functional impairment is so


    severe that replacement therapy is indicated
    DEFINITION
    The AKIN network

    an abrupt (within 48 hours) reduction in kidney function:

    - absolute increase in SCr of >0.3 mg/dL ( >25 μmol/L)

    -a percentage increase of 50%

    -a reduction in urine output (documented oliguria of < 0.5


    mL/kg/hr for >6 hours).
    The pathogenesis of AKI is complex

    • mismatch oxygen+ nutrient delivery to the nephrons vs energy


    demand of the nephrons local or generalized ischemia

    • tissue injury and organ dysfunction


    increased levels of inflammatory mediators

    endothelial damage
    leukocyte- endothelial adhesion
    (particularly in the postcapillary venules)

    activating the coagulation pathways


    small-vessel occlusion

    oxygen&nutrient delivery to epithelial cells


    Symptoms and Signs

    • Azotemia nausea, vomiting, malaise, altered sensorium.

    • Hypertension is rare, but fluid homeostasis is often altered.

    • Hypovolemia/hypervolemia, platelet dysfbleeding

    • Arrhythmias  hyperkalemia

    • Rales hypervolemia, Pericardial effusions  azotemia

    • encephalopathic changes with asterixis+confusion; seizures


    Laboratory exam
    • Elevated BUN and creatinine

    • Hyperkalemia, Hyperphosphatemia, Hypocalcemia

    • ECG  peaked T waves, PR prolongation, QRS widening

    • A long QT segment hypocalcemia

    • Anion gap metabolic acidosis

    • Anemia, platelet dysfunction


    ACUTE OR CHRONIC???
    PRE, RENAL, OR POST RENAL??
    postrenal azotemia
    • bladder ultrasonography and bladder catheterization if
    hydroureter and hydronephrosis are present along with an
    enlarged bladder

    • Rarely, obstruction is not diagnosed by ultrasonography.


     a CT scan or MRI
    tested in only small studies and limited
    clinical situations. No cutoff
    value . Very limited data available, at present,
    about temporal expression patterns
    Management principles in ARF

    • Identify and correct pre-renal & post-renal factors

    • Optimise cardiac output and renal blood flow

    • Review drugs: stop nephrotoxic agents; adjust


    doses and monitor concentrations

    • Monitor fluid balance and daily body weight

    • Identify and treat acute complications


    (hyperkalaemia, acidosis, pulmonary oedema)

    BMJ 2006;333;786-790
    Management principles in ARF

    • Nutritional support: adequate calories, minimal


    nitrogenous waste, potassium restriction

    • Identify and aggressively treat infection; minimise


    indwelling lines; remove bladder catheter if anuric

    • Identify&treat bleeding tendency:prophylaxs PPI/H2


    antagonist, transfuse if required, avoid aspirin

    • Dialysis
    BMJ 2006;333;786-790
    INDICATION FOR RRT
    Life-threatening
    complications of acute
    kidney injury (AKI)
    Refractory
    •initiation of RRT
    fluid overload

    Hyperkalemia
    •(Grade 1A). (plasma potassium concentration
    >6.5 meq/L)/rapidly rising potassium levels

    • Signs of uremiapericarditis, neuropathy, or


    Whether initiation of
    unexplained decline in mental status
    earlier or prophylactic

    • Metabolic acidosis (pH lessdialysis offers any clinical


    than 7.1)
    or survival benefit is
    unproven
    WHICH RRT IS BETTER?
    • Survival and recovery of renal function are
    similar with both CRRT and IHD.

    • Data do not support the superiority of any mode

    • Selection: local expertise, staff and equipment

    • Acute brain injury or fulminant hepatic failure


    continuous therapy  better preservation of
    cerebral perfusion
    WHICH RRT IS BETTER?

    • ATN studyintermittent HD 3 times/week, minimum


    delivered Kt/V of 1.2/treatment Grade 1B).

    • NO evidence frequent hemodialysis associated with


    improved outcomes

    • CRRT venovenous circuits more recommended


    than arteriovenous circuits (Grade 1B) with effluent
    flow rate at least 20 mL/kg per hour (Grade 1B)
    \

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